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In Vivo Study of Human Endothelial-Pericyte Interaction Using the Matrix Gel Plug Assay in Mouse
Published on: December 19, 2016
Ena/VASP is required for endothelial barrier function in vivo
Craig Furman1, Alisha L Sieminski, Adam V Kwiatkowski
1Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
The Journal of Cell Biology
|November 14, 2007
Summary
Vasodilator-stimulated phosphoprotein (Ena/VASP) proteins are crucial for maintaining blood vessel integrity. Their absence in vivo causes severe vascular defects, leading to embryonic lethality and highlighting their role in endothelial cell function.
Area of Science:
- Cell Biology
- Biochemistry
- Developmental Biology
Background:
- Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) proteins are regulators of actin dynamics.
- Ena/VASP proteins are found at sites of actin remodeling, such as cellular protrusions and junctions.
- Previous studies suggest Ena/VASP involvement in cellular junction formation and function.
Purpose of the Study:
- To investigate the in vivo role of Ena/VASP proteins in endothelial junctions.
- To determine the consequences of Ena/VASP deficiency in the vasculature.
Main Methods:
- Analysis of Ena/VASP-deficient animal models.
- Assessment of endothelial cell F-actin content and actomyosin contractility.
- Evaluation of endothelial cell response to shear stress.
Main Results:
- Ena/VASP deficiency leads to vascular patterning defects and loss of structural integrity.
- Absence of Ena/VASP results in edema, hemorrhaging, and embryonic lethality.
- Ena/VASP activity is essential for normal F-actin content, actomyosin contractility, and shear stress response in endothelial cells.
Conclusions:
- Ena/VASP proteins are critical for maintaining functional endothelia.
- Ena/VASP is vital for actin cytoskeleton remodeling events that support endothelial cell structure and function.
- This study underscores the importance of Ena/VASP in vascular development and integrity.
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